ArticleThe EMBO journal2021
PECAM-1 supports leukocyte diapedesis by tension-dependent dephosphorylation of VE-cadherin.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- The Impact of Antigen Presentation on BBB Disruption and Neuroinflammation.Physiology (Bethesda, Md.) · 2026Review
- Molecular control of platelet extravasation into tumors and its impact on tumor growth.Blood vessels, thrombosis & hemostasis · 2026Article
- ZEB1 Modifies VE-Cadherin Signaling in Lymphatic Endothelial Cells.Microcirculation (New York, N.Y. : 1994) · 2026Article
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Plakoglobin transmits tension across VE-cadherin for vascular leak formation and leukocyte diapedesis.The EMBO journal · 2026Article
- SHP2 regulates VEGFR2 Y1175/PLCγ signaling to impair tumor endothelial barrier stability.iScience · 2026Article
- Mechanoresponsive ion channels Piezo1 and TRPV4 stimulate ADAM10 and ADAM17 with differential impact on endothelial migration and proliferation.Cell communication and signaling : CCS · 2026Article
- Identification of key biomarkers for myocardial infarction by multi-omics analysis and machine learning.Frontiers in immunology · 2026Article
- Article
- Extracellular matrices regulate extravasation journey of leukocytes and inflammatory tissue fate.eLife · 2025Review
- Distinct VE-cadherin serine and tyrosine phosphorylation sites and their role for inflammation-induced vascular permeability in vivo.Cellular and molecular life sciences : CMLS · 2025Article
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- TNF-α induces VE-cadherin-dependent gap/JAIL cycling through an intermediate state essential for neutrophil transmigration.Frontiers in immunology · 2025Article
- Vascular endothelial cadherin dysfunction: A predictor of hypertensive nonlobar intracerebral hemorrhage.Surgical neurology international · 2025Article
- VE-cadherin RGD motifs are dispensable for cell-cell junctions, endothelial barrier function and monocyte extravasation.Tissue barriers · 2025Article
- Membrane Tension Regulation is Required for Wound Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- SHP2-Triggered Endothelial Cell Activation Fuels Estradiol-Independent Endometrial Sterile Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- An Intriguing Structural Modification in Neutrophil Migration Across Blood Vessels to Inflammatory Sites: Progress in the Core Mechanisms.Cell biochemistry and biophysics · 2024Review
- Csk controls leukocyte extravasation via local regulation of Src family kinases and cortactin signaling.Frontiers in immunology · 2024Article
- Immune disease dialogue of chemokine-based cell communications as revealed by single-cell RNA sequencing meta-analysis.Frontiers in systems biology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukocyte extravasation is an essential step during the immune response and requires the destabilization of endothelial junctions. We have shown previously that this process depends in vivo on the dephosphorylation of VE-cadherin-Y731. Here, we reveal the underlying mechanism. Leukocyte-induced stimulation of PECAM-1 triggers dissociation of the phosphatase SHP2 which then directly targets VE-cadherin-Y731. The binding site of PECAM-1 for SHP2 is needed for VE-cadherin dephosphorylation and subsequent endocytosis. Importantly, the contribution of PECAM-1 to leukocyte diapedesis in vitro and in vivo was strictly dependent on the presence of Y731 of VE-cadherin. In addition to SHP2, dephosphorylation of Y731 required Ca
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.